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Silicon dioxide (SiO(2)) is conventionally reduced to silicon by carbothermal reduction, in which the oxygen is removed by a heterogeneous-homogeneous reaction sequence at approximately 1,700 degrees C. Here we report pinpoint and bulk electrochemical methods for removing oxygen from solid SiO(2) in a molten CaCl(2) electrolyte at 850 degrees C. This approach involves a 'contacting electrode', in which a metal wire supplies electrons to a selected region of the insulating SiO(2). Bulk reduction of SiO(2) is possible by increasing the number of contacting points. The same method was also demonstrated with molten LiCl-KCl-CaCl(2) at 500 degrees C. The novelty and relative simplicity of this method might lead to new processes in silicon semiconductor technology, as well as in high-purity silicon production. The methodology may be applicable to electrochemical processing of a wide variety of insulating materials, provided that the electrolyte dissolves the appropriate constituent ion(s) of the material.

Chronic renal failure may occur in etiologically diverse renal diseases and can be caused by hemodynamic, immunologic and metabolic factors. Initial damage may evoke irreversible scarring, which involves production of a number of proinflammatory and fibrogenic cytokines, including platelet-derived growth factor (PDGF) and transforming growth factor beta (TGF-beta). Connective tissue growth factor (CTGF), a cytokine of the family of growth regulators comprising sef10, cyr61, CTGF and nov, has recently been described in association with scleroderma and other scarring conditions. We investigated CTGF mRNA expression in 65 human renal biopsy specimens of various renal diseases by in situ hybridization. In control human kidney CTFG mRNA was mainly expressed in visceral epithelial cells, parietal epithelial cells, and some interstitial cells. Connective tissue growth factor was strongly up-regulated in the extracapillary and severe mesangial proliferative lesions of crescentic glomerulonephritis, IgA nephropathy, focal and segmental glomerulosclerosis and diabetic nephropathy. An increase in the number of cells expressing CTGF mRNA was observed at sites of chronic tubulointerstitial damage, which correlated with the degree of damage. in the tubulointerstitial area the majority of the CTGF mRNA positive cells coexpressed alpha-smooth muscle actin, and were negative for macrophage markers. Our results indicate that CTGF may be a common growth factor involved in renal fibrosis.

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